Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have previously shown that renal vascular resistance is less in Dahl salt-sensitive rats than salt-resistant rats fed 1% NaCl diets; however, renal vascular resistance increases before nonrenal vascular resistance as salt-sensitive rats develop hypertension when fed 8% NaCl diets. When salt-resistant rats are given 8% NaCl diets, renal vascular resistance decreases. The current study reports effects of atrial natriuretic peptide, nitroprusside, norepinephrine, angiotensin II, and endothelin-1 on renal and nonrenal vascular resistance in prehypertensive salt-sensitive and salt-resistant rats given 1% NaCl diets; doses used did not affect blood pressure. Resistance of nonrenal vessels in salt-sensitive and salt-resistant rats responded similarly to dilators or constrictors. However, atrial natriuretic peptide and nitroprusside decreased renal vascular resistance of salt-resistant rats (by 65%, p less than 0.01) but not that of salt-sensitive rats. Norepinephrine, angiotensin II, and endothelin-1 increased renal vascular resistance in salt-sensitive rats by 126%, 135%, and 135%, respectively (p less than 0.01); norepinephrine and angiotensin II did not change renal vascular resistance of salt-resistant rats, but endothelin-1 decreased renal vascular resistance in salt-resistant rats by 30% (p less than 0.01). Reactivity of nonrenal blood vessels in prehypertensive salt-sensitive and salt-resistant rats was similar when infused with dilators or constrictors in doses used. By contrast, renal vessels of salt-sensitive rats did not dilate in response to atrial natriuretic peptide and nitroprusside but were hypersensitive to norepinephrine and angiotensin II. Endothelin-1 caused renal vasoconstriction in salt-sensitive rats and renal vasodilation in salt-resistant rats.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1992 Oct
PMID:Impaired renal vascular reactivity in prehypertensive Dahl salt-sensitive rats. 139 88

Submaximal exercise provokes an abnormal elevation in albuminuria in type 1 (insulin-dependent) diabetes mellitus. Plasma catecholamines might be involved in this phenomenon by a renal vasoconstrictive effect. Twelve healthy subjects (Controls: albuminuria < 10 micrograms min-1), 13 normoalbuminuric type 1 diabetic patients (DNormo: albuminuria < 10 micrograms min-1) and 13 microalbuminuric type 1 diabetic patients (DMicro: albuminuria 10-200 micrograms min-1) performed a fixed bicycle workload (600 kpm for 20 min+urine collection 40 min post exercise). None of the patients suffered from autonomic neuropathy or hypertension. Fractional albumin clearance (FalbCl) rose in DNormo (p = 0.02) and DMicro (p = 0.01) but not in the Controls (p = 0.40). Basal plasma adrenaline and noradrenaline were not different in the three groups. The increments in noradrenaline were more pronounced in DNormo and DMicro than in Control (Controls < DNormo, p < 0.05; Controls < DMicro, p < 0.01). The changes in FalbCl were significantly correlated with the changes in noradrenaline (all subjects r = 0.65, p < 0.001). The increments in adrenaline were not different in the diabetic groups compared to the controls, and were not related to the changes in FalbCl. Multiple regression analysis showed that changes in plasma noradrenaline (p < 0.002) and in mean arterial pressure (p < 0.005) independently contributed to the changes in FalbCl (multiple r = 0.73). It is concluded that the exercise-induced plasma noradrenaline response is increased in normo- and microalbuminuric type-1 diabetic patients. Noradrenaline appears to contribute in the exercise-induced changes in renal protein handling, possibly by its effect on renal haemodynamics.
 ...
PMID:Abnormal plasma noradrenaline response and exercise induced albuminuria in type 1 (insulin-dependent) diabetes mellitus. 148 18

Correlation between increased cranial and peripheral norepinephrines and increased cranial to systemic renin ratio has been observed in a small number of patients with postcarotid endarterectomy hypertension. In an effort to confirm these findings, we studied cranial and peripheral levels of catecholamines and peripheral renin activity in 120 consecutive carotid endarterectomies. Samples were taken before carotid clamping (Sample I) and just after clamp release (Sample II). Norepinephrine, epinephrine and dopamine values did not correlate with postcarotid endarterectomy hypertension. There was no association between peripheral renin values and postcarotid endarterectomy hypertension.
 ...
PMID:The role of renin and catecholamine production in postcarotid endarterectomy hypertension. 154 35

The authors analysed the dynamics of the activity of the renin-angiotensin-aldosterone, hypophyseal-adrenal, and sympathoadrenal systems in 46 patients during a hemodialysis session according to the type of hemodynamics. No essential changes were encountered in the hormone concentration in patients with normotension and "controllable" hypertension. In patients with "uncontrollable" hypertension the dialysis dehydration was attended by increased activity of the renin-angiotensin-aldosterone system, the level of cortisol and the adrenocorticotropic hormone increased slightly. Daily catecholamine excretion was 2-3.5 times below the lowest normal value. Noradrenaline clearance of the plasma membrane dialyser was 82.1 ml/min. Increase in the concentration of noradrenaline, and the activity of renin and aldosterone were encountered both in hypotension and in arterial hypertension. It is concluded that disturbed water balance, dyselectrolythemia, anemia, infectious complications, etc. are the trigger factor of decompensation of the system of the hormonal hemodynamic regulation. Substitution adrenomimetic therapy for arresting collaptoid reactions is inexpedient. Systematic use of medicinal agents should be avoided in favour of a search for an optimal dialysis regimen, should this prove ineffective the decision should be made in favour of an operation.
 ...
PMID:[The activities of the renin-angiotensin-aldosterone and sympathetic-adrenal systems during hemodialysis]. 165 15

In essential hypertension sympathetic nerve firing is commonly increased. A central nervous system origin has been presumed but not tested directly. To estimate cerebral norepinephrine release in essential hypertension, spillover of norepinephrine into the cerebrovascular circulation was measured by isotope dilution, with high internal jugular venous sampling. Norepinephrine was released into the cerebrovascular circulation in both hypertensive patients and healthy volunteers and was present after administration of the ganglion blocker trimethaphan and in patients with sympathetic nervous failure, indicating that brain neurons and not cerebrovascular sympathetic nerves were the probable source. Although differing among hypertensive patients, norepinephrine spillover on average was higher in the hypertensive patients (153 +/- 41 pmol/min) than in healthy subjects (59 +/- 12 pmol/min; p less than 0.05), and was elevated in six of 17 patients, in whom the accompanying whole body norepinephrine spillover rate was higher than in the remaining 11 patients (p less than 0.01). To test for a possible link between brain norepinephrine release and human sympathetic nervous function, the effect of the tricyclic antidepressant desipramine (0.3 mg/kg i.v.) on both brain and whole body norepinephrine spillover was measured in healthy volunteers. Desipramine lowered the cerebrovascular spillover of norepinephrine, its precursor dihydroxyphenylalanine, and its metabolite dihydroxyphenylglycol by 50-80% and produced a mean fall of 35% in whole body norepinephrine spillover. One interpretation of these results is that human sympathetic nerve firing is dependent on norepinephrine release within the brain and that increased cerebral norepinephrine release may possibly be present in some patients with essential hypertension, underlying their higher sympathetic nerve firing rates.
Hypertension 1992 Jan
PMID:Increased norepinephrine spillover into the jugular veins in essential hypertension. 173 Apr 41

Norepinephrine-induced responses in isolated perfused mesenteric vascular bed from normotensive and renovascular hypertensive rats were examined in the presence of adenosine diphosphate (ADP, 2 x 10(-6) M). Responses to norepinephrine were significantly greater in vessels from hypertensive rats. Norepinephrine-induced contractions increased after the removal of endothelium. N omega-Nitro-L-arginine (L-NOARG), a potent inhibitor of nitric oxide formation, similarly increased contractions. The greatest responses were obtained, however, after treatment of the vascular segments with methylene blue. The presence of ADP caused significant endothelium-dependent decreases in contractions. Although decreases caused by ADP in vessels with endothelium after treatment with L-NOARG were not statistically significant, a tendency to decreased responses seems to suggest that L-NOARG diminishes but does not completely prevent the effect of ADP in mesenteric vessels. Methylene blue partially reduced the endothelium-dependent ADP-induced relaxant effects in sham-operated nephrectomized rats. A tendency to increased contractions to norepinephrine was observed in the presence of ADP after removal of endothelium. Thus, in the mesenteric resistance arteries of the rat under stimulation by ADP, it appears that nitric oxide released from L-arginine and the activity of soluble guanylate cyclase account only in part for the endothelium-dependent decreased responses to norepinephrine. When nitric oxide formation or soluble guanylate cyclase activity are depressed simultaneously with endothelium damage, ADP released from platelets or red blood cells may be an important factor that acts synergically with vasoconstrictor stimuli.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1992 Feb
PMID:Endothelium-dependent and endothelium-independent effects of adenosine diphosphate in renovascular hypertension. 173 85

The effect of chronic alcohol administration on blood pressure was investigated in 7-week-old Wistar rats. Tail-cuff blood pressure was significantly higher in rats who received 15% ethanol in drinking water than in control rats. Intracellular free calcium concentration of lymphocytes was increased, while magnesium concentration of erythrocyte, aorta, and skeletal muscle and erythrocyte ouabain-sensitive 22Na efflux rate constant (Kos) were decreased in alcohol-induced hypertensive rats but not in control rats. Extracellular fluid volume was also increased in alcohol-administered rats. Oral magnesium supplementation (1% MgO in rat chow) attenuated the development of alcohol-induced hypertension accompanied by increased magnesium concentration of erythrocyte, aorta, skeletal muscle, and Kos and decreased intraerythrocyte sodium concentration. Norepinephrine half-life time of the heart and spleen was also increased in magnesium-supplemented rats. Blood pressure significantly correlated positively with intracellular calcium concentration and extracellular fluid volume, negatively with magnesium concentration of erythrocyte, aorta, skeletal muscle, and Kos. These results suggest that increased intracellular calcium, which was partly due to magnesium depletion and suppressed sodium pump activity, and expanded body fluid volume had a possible role in the development of alcohol-induced hypertension. It is also suggested that oral magnesium supplementation had a hypotensive effect on alcohol-induced hypertension possibly through decreased intracellular sodium concentration caused by an activation of sodium pump and decreased sympathetic nervous activity.
Hypertension 1992 Feb
PMID:Magnesium supplementation prevents the development of alcohol-induced hypertension. 173 52

Total inositol phosphate (IP) formation was measured in the aorta and femoral artery from rabbits at 1, 2, and 6 weeks after kidney wrapping, at which times the mean arterial pressures were 88 +/- 4, 96 +/- 3 and 126 +/- 7 (control = 74 +/- 3) mmHg. Noradrenaline (10(-7)-10(-4) M)-stimulated IP formation was increased in the aorta and femoral artery from hypertensive rabbits at 2 weeks (e.g., aorta noradrenaline 10(-6) M sham = 105 +/- 14%, hypertensive = 164 +/- 20% of control). In contrast, endothelin-1-stimulated IP formation was unchanged at 2 weeks. Noradrenaline-stimulated IP formation was unchanged at 1 and 6 weeks. Basal IP formation was not significantly different in normotensive and hypertensive animals. In perinephritis hypertension, there is an alteration in phosphatidylinositol metabolism in arterial smooth muscle at the time when blood pressure is rising rapidly. This alteration may affect a specific phosphatidylinositol pool that is linked to the alpha-adrenoceptor but not to the endothelin-1 receptor.
 ...
PMID:Noradrenaline and endothelin-stimulated inositol phosphate formation in arterial smooth muscle from rabbits with perinephritis hypertension. 179 9

Noradrenaline, adrenaline and mean arterial pressure prior to and 3 hours after clonidine administration were evaluated in order to assess a value of single dose of 0.3 mg clonidine in the diagnosis of pheochromocytoma. The study involved 12 patients with pheochromocytoma, 17 patients with arterial hypertension, and 9 patients with borderline hypertension. Seven healthy volunteers served as a control group. It was found that clonidine decreased noradrenaline levels in all healthy subjects and patients with the primary blood hypertension and did not affect noradrenaline levels in patients with pheochromocytoma. Clonidine decreased noradrenaline levels in two patients with normal resting noradrenaline levels. Simultaneously, clonidine decreased noradrenaline levels in two patients with normal resting levels of this catecholamine. The obtained results indicate low specificity of the clonidine test and its value in the diagnosis of pheochromocytoma in patients with normal noradrenaline blood levels.
 ...
PMID:[Test with clonidine for diagnosing pheochromocytoma]. 184 84

This study was designed to examine the effects of fetal hypertension on the umbilical artery pulsatility index. Fetal arterial blood pressure and umbilical venous pressure were measured in eight sheep, 3 to 5 days after surgery. Umbilical blood flow was measured with an electromagnetic flowmeter around the common umbilical vein. Umbilical artery flow velocity waveforms were obtained either by an indwelling 5 MHz pulsed Doppler device (n = 4) or transcutaneously by a 4 MHz continuous-wave Doppler device (n = 4). Fetal blood pressure was raised by intravenous infusion of norepinephrine 10 micrograms/min during 5 minutes. Norepinephrine infusion resulted in elevated arterial and umbilical venous pressures, accompanied by a bradycardia during the first 3 minutes. Umbilical blood flow, calculated placental vascular resistance, and umbilical artery pulsatility index did not change. After atropine administration, the norepinephrine-induced elevated arterial and umbilical venous pressures were accompanied by tachycardia, increased umbilical blood flow, and no change in placental vascular resistance and umbilical artery pulsatility index. It is concluded that fetal arterial hypertension provoked by norepinephrine infusion has no effect on placental vascular resistance, umbilical blood flow, and umbilical artery pulsatility index.
 ...
PMID:Fetal hypertension induced by norepinephrine infusion and umbilical artery flow velocity waveforms in fetal sheep. 187 57


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>